Cerebral bleeding affects about 2.5 per 10,000 people each year.[2] It occurs more often in males and older people.[2] About 44% of those affected die within a month.[2] A good outcome occurs in about 20% of those affected.[2]Strokes were first divided into their two major types, bleeding and insufficient blood flow, in 1823.[5]

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People with intracerebral bleeding have symptoms that correspond to the functions controlled by the area of the brain that is damaged by the bleed.[6] Other symptoms include those that indicate a rise in intracranial pressure caused by a large mass putting pressure on the brain.[6]
Intracerebral bleeds are often misdiagnosed as subarachnoid hemorrhages due to the similarity in symptoms and signs. A severe headache followed by vomiting is one of the more common symptoms of intracerebral hemorrhage. Another common symptom is a patient can collapse. Some people may experience continuous bleeding from the ear. Some patients may also go into a coma before the bleed is noticed.

Traumautic intracerebral hematomas are divided into acute and delayed. Acute intracerebral hematomas occur at the time of the injury while delayed intracerebral hematomas have been reported from as early as 6 hours post injury to as long as several weeks.

Intraparenchymal hemorrhage can be recognized on CT scans because blood appears brighter than other tissue and is separated from the inner table of the skull by brain tissue. The tissue surrounding a bleed is often less dense than the rest of the brain because of edema, and therefore shows up darker on the CT scan.[14]

When due to high blood pressure, intracerebral hemorrhages typically occur in the putamen (50%) or thalamus (15%), cerebrum (10-20%), cerebellum (10-13%), pons (7-15%), or elsewhere in the brainstem (1-6%).[15][16]

Giving Factor VIIa within 4 hours limits the bleeding and formation of a hematoma. However, it also increases the risk of thromboembolism.[17] It thus overall does not result in better outcomes in those without hemophilia.[22]

The risk of death from an intraparenchymal bleed in traumatic brain injury is especially high when the injury occurs in the brain stem.[27] Intraparenchymal bleeds within the medulla oblongata are almost always fatal, because they cause damage to cranial nerve X, the vagus nerve, which plays an important role in blood circulation and breathing.[9] This kind of hemorrhage can also occur in the cortex or subcortical areas, usually in the frontal or temporal lobes when due to head injury, and sometimes in the cerebellum.[9][28]

For spontaneous ICH seen on CT scan, the death rate (mortality) is 34–50% by 30 days after the insult,[7] and half of the deaths occur in the first 2 days.[29] Even though the majority of deaths occurs in the first days after ICH, survivors have a long term excess mortality of 27% compared to the general population.[30]

The inflammatory response triggered by stroke has been viewed as harmful in the early stage, focusing on blood-borne leukocytes, neutrophils and macrophages, and resident microglia and astrocytes.[32] A human postmortem study shows that inflammation occurs early and persists for several days after ICH.[33] Modulating microglial activation and polarization might mitigate intracerebral hemorrhage-induced brain injury and improve brain repair.[34] A new area of interest is the role of mast cells in ICH.[35]